XPOT (exportin for tRNA) is a nuclear export receptor that mediates the transport of aminoacylated tRNAs from the nucleus to the cytoplasm. The protein functions by binding to tRNA and the GTPase Ran in its active GTP-bound form, forming a trimeric complex that docks to nuclear pore complexes through nucleoporin interactions 1. Upon cytoplasmic transit, complex disassembly and Ran-GTP hydrolysis cause tRNA release, allowing XPOT to return to the nucleus for additional transport cycles. Beyond its canonical tRNA export function, XPOT has emerged as a significant factor in cancer biology. Overexpression of XPOT is associated with poor prognosis in multiple cancer types, including neuroblastoma, hepatocellular carcinoma, and breast cancer 234. In triple-negative breast cancer, XPOT specifically regulates nuclear export of select tRNA isodecoders, particularly tRNA-Ala-AGC-10-1, which drives translation of TTC19 protein essential for cytokinesis 4. XPOT knockdown inhibits tumor cell proliferation, migration, and invasion by causing cell cycle arrest and cytokinesis failure 34. Additionally, XPOT can mediate unconventional nuclear export of transcription factors like NFAT5 under specific cellular conditions 1. These findings position XPOT as both a critical cellular transport protein and potential therapeutic target in cancer treatment.